Isoimmunization of marmosets with marmoset (interspecies) platelet preparations leads to severe thrombocytopenia and frequently death of the animal. The presence of antibodies directed toward the donor but not host-type platelet antigens offers a remarkable parallel to the clinical disorder of posttransfusion purpura (PTP) of man. Induction of the disease in the marmoset appears to be related to an active deposition of IgG on the host's platelets preceding development of thrombocytopenia, this finding analogous to a similar demonstration made for idiopathic thrombocytopenic purpura (ITP). The marmoset, therefore, offers a potentially excellent animal model for two clinical disease entities bearing on the problem of autoimmune thrombocytopenia. The objective of the present study is to define the humoral and cellular components involved in the pathogenesis of the induced disease and thereby gain insight concerning the etiology and treatment of clinical PTP and ITP. To achieve this objective, both in vitro and in vivo studies are planned: (1) to develop immunization protocols predictably leading to thrombocytopenia and ultimate maintenance of the host's platelets in an IgG-positive state, (2) define humoral components associated with the disease placing emphasis on the role of soluble antigen-antibody complexes, (3) determine the cellular events that are involved in the pathogenesis of the disease in vivo, (4) to attempt therapy by splenectomy and immunosuppressive procedures, and (5) perform immunofluorescent histopathology on selected tissues to gain further insight on the in vivo events leading to manifestation of the disease. The results of our study should provide a unique animal model that is currently lacking for the problem of immunologic thrombocytopenia in man.